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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxygen consumption in blood platelets of 14 pituitary dwarfs aged from 2 to 8 years was investigated before and after a 2 months' treatment with growth hormone (GH). No significant difference was found between dwarfs and control subjects in respect of basal platelet oxygen uptake (4.0 +/- 3.8 mmol O2/10(9) platelets/min in dwarfs as against 6.4 +/- 4.1 in controls), but the abrupt increase in oxygen consumption induced by thrombin was significantly reduced in dwarfs (4.3 +/- 4.1) as compared with controls (12.3 +/- 7.6; p less than 0.01). During GH treatment, however, the dwarfs' response to thrombin stimulation was similar to that of controls. Since dwarfs had normal platelet malonyldialdehyde production, it is likely that the mitochondrial component of thrombin-induced high oxygen consumption was deficient. These results suggest that blood platelets may contribute to the protective effect of GH deficiency against atherosclerosis.
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PMID:[Blood platelet oxygen consumption in pituitary dwarfs (author's transl)]. 725 37

The large vessel disease develops slowly and progressively among most diabetics. According to the concept of a specific diabetic macroangiopathy, the alterations in the large vessels are part of the general diabetic angiopathy and are different from the spotty atherosclerosis. This hypothesis proposes that the changes develop a consequence of the metabolic situation in diabetes. The concept is based on epidemiologic, clinical, and patho-anatomical observations. A model of large-vessel disease in diabetes is briefly described. Diabetic serum causes proliferation of the aortic myomedial cells in culture. Growth hormone causes a similar proliferation. Type 1 procollagen and fibronectin elaboration is enhanced by diabetic serum. The same effect has been found with growth hormone. Insulin treatment in experimental diabetes prevents the proliferation of arterial myomedial cells in the coronary arteries. The presented data are compatible with the concept of a diabetic macroangiopathy distinct from atherosclerosis.
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PMID:Diabetic macroangiopathy and growth hormone. 729 69

Serum factors from non-ketotic poorly controlled diabetic patients when compared to serum factors from normal subjects, stimulate growth and protein synthesis of cultured fibroblasts from diabetic patients by 25-50%. This increased growth stimulating effect of diabetic serum is mainly related to low molecular weight components (mol. wt. < 12,000 daltons), but not to insulin or glucose. These low molecular weight components of diabetic serum are effective only in combination with serum factors of a molecular weight > 12,000 daltons which are essential for initiation and continuous stimulation of cellular growth. As the growth stimulation by diabetic serum factors with a molecular weight < 12,000 daltons does not differ from comparable normal serum factors, the relevance of these serum factors (e.g. growth hormone, lipoproteins) for the increased growth stimulation of mesenchymal cells in diabetes mellitus seems to be only of limited importance. In as much as these in vitro results represent the in vivo situation, chronic exposure of vascular cells from diabetics to these serum factors could be related to the increased angiopathic risk in diabetes mellitus.
Atherosclerosis 1980 Oct
PMID:Increased growth stimulation of fibroblasts from diabetics by diabetic serum factors of low molecular weight. 742 4

Hypophysectomy was found to increase low density lipoprotein (LDL) cholesterol in rats from 0.18 to 1.18 mmol/l in 1 week, while very low density lipoprotein (VLDL) and high density lipoprotein (HDL) cholesterol decreased simultaneously from 0.08 to 0.03 mmol/l and from 2.12 to 1.01 mmol/l, respectively. Serum total cholesterol levels remained unchanged. Thyroid supplementation (T3 or T4) with doses causing a euthyroid state did not fully correct the lipoprotein pattern. The increase of LDL caused by hypophysectomy was significantly rectified, but the normal level could not be maintained, whilst the HDL level was not at all affected by thyroid hormones. Serum total cholesterol was markedly reduced in all groups with thyroid supplementation, indicating increased cholesterol catabolism. These results suggest that TSH and peripheral thyroid hormones modulate LDL but no effect on HDL could be detected. Other hormones, notably ACTH, growth hormone, lipotropins and gonadotropins are also involved in the control of lipoproteins at the pituitary level. Their exact impact cannot at present be assessed.
Atherosclerosis
PMID:Failure of thyroid hormones to maintain the normal lipoprotein pattern in rats after removal of the pituitary gland. 747 Jan 94

Untreated acromegaly is associated with an increased cardiovascular morbidity and mortality. The contribution of altered lipid metabolism remains unclear. We investigated the relationship between serum apolipoprotein(a) (apo(a)) and growth hormone (GH) levels in 15 patients with acromegaly before and during treatment with octreotide, a long-acting somatostatin analogue, 288-600 micrograms/day s.c., for 6 months. Before treatment serum apo(a) was significantly elevated in acromegalic patients (geometric mean being 323 U/l vs. 142 U/l in controls (n = 92; P < 0.01)). Octreotide treatment resulted in significant reductions in serum apo(a) concentration (F = 7.22; P < 0.01; geometric mean being 232 U/l and 248 U/l at 3 months and 6 months respectively) and apo(a) concentrations on treatment were not significantly different from control values. There were significant reductions in serum GH (F = 7.30; P < 0.01), insulin growth factor 1 (IGF1) (F = 31.4, P < 0.001) and insulin (F = 4.57; P < 0.05) concentrations. Plasma glycosylated haemoglobin levels were unchanged. Apo(a) levels correlated with serum GH (r = 0.450; P < 0.01) but showed no correlation with basal insulin concentrations. Serum HDL cholesterol increased on treatment (F = 4.29; P < 0.05). Triglycerides were reduced only in the 12 patients without diabetes mellitus (F = 4.75; P < 0.05). No significant change in LDL cholesterol occurred. Our findings suggest that apo(a) may constitute another cardiovascular risk factor in untreated acromegaly and that GH may be involved in the regulation of circulating apo(a) concentration.
Atherosclerosis 1993 Dec
PMID:Serum apolipoprotein(a) correlates with growth hormone levels in Chinese patients with acromegaly. 814 41

Altered homocysteine metabolism is implicated as a pathogenic factor in atherogenesis, neoplasia, and aging. Hereditary enzymatic deficiencies and nutritional deficiencies of folate, pyridoxine, or cobalamin are associated with elevated blood homocysteine, accelerated atherosclerosis, and manifestations of aging. The failure of malignant cells to metabolize homocysteine thiolactone to sulfate is attributed to deficiency of thioretinaco, a complex containing cobalamin, homocysteine thiolactone, and retinoic acid. The sulfhydryl group of homocysteine is believed to act catalytically with ferric or cupric ions in a mixed function oxidation system to generate hydrogen peroxide, oxygen radicals, and homocysteinyl radicals. These reactive species may interact with the active site of enzyme protein to cause inactivation of catalytic activity. Homocysteine thiolactone is oxidized to sulfate by a process involving ascorbate, thioretinamide, and superoxide, under the control of thyroxine and growth hormone. Thioretinaco is believed to be the active site of adenosine triphosphate (ATP) binding in oxidative phosphorylation with the participation of oxygen, ascorbate, proton gradient, and electron transport. Depletion of thioretinaco from mitochondrial and microsomal membranes may be associated with increased formation and release of radical oxygen species within neoplastic and senescent cells. Specific proposals are made for investigating the importance of homocysteine metabolism in the oxidative modification of proteins and lipids.
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PMID:Homocysteine metabolism and the oxidative modification of proteins and lipids. 832 40

Recombinant human growth hormone (rhGH) is now available for treatment of short stature due to growth hormone (GH) deficiency. It's potential use in other causes of short stature raises concerns about adverse effects of long term treatment on carbohydrate and lipoprotein metabolism. We describe the serial changes in lipids, lipoproteins and apolipoproteins, including apo(a) in 12 children with beta-thalassaemia major undergoing rhGH treatment for 24-36 months. All showed satisfactory increases in height and weight. A significantly higher mean plasma apo(a) was observed at 3 months (102.6 U/l) versus baseline (71.4 U/l, P < 0.01, geometric means). Subsequently apo(a) levels gradually decreased returning to pretreatment levels after 36 months of rhGH treatment. There were parallel rises and falls in the apo(a) isoforms of different sizes during treatment. There were only minimal changes in the other lipid related parameters. All children had markedly reduced cholesterol levels (3.0 +/- 0.49 mmol/l, mean +/- S.D.) characteristic of their underlying disease. In conclusion the elevation of apo(a) by GH is only transient, there is no differential effect of rhGH on the large and small isoforms of apo(a) and there are no clinically significant adverse effects of rhGH treatment on lipoprotein metabolism.
Atherosclerosis 1997 Feb 10
PMID:Growth hormone therapy transiently increases apolipoprotein(a) in short beta-thalassaemia major children with normal growth hormone reserve. 905 Jul 74

Acromegaly is associated with changes in lipoprotein metabolism and an excess in cardiovascular mortality. We have examined low density lipoprotein (LDL) subfraction distribution in 24 patients with active acromegaly and in controls matched for age, sex and body mass index. LDL was subfractionated by density gradient ultracentrifugation. The concentration of small dense LDL-III was significantly higher in the acromegalic patients compared to the controls (94.2 +/- 44.9 versus 67.2 +/- 30.4 mg/dl, P < 0.05) and there was a concomitant reduction in the intermediate subfraction LDL-II (124.8 +/- 31.3 versus 149.9 +/- 30.0 mg/dl, P < 0.05). Univariate analysis showed that both growth hormone (GH) and insulin-like growth factor (IGF)-I correlated with LDL-III and inversely with LDL-II. Acromegalic patients were found to have lower hepatic lipase (HL) and lipoprotein lipase (LPL) activities than controls (HL: 13.29 +/- 6.56 versus 21.58 +/- 7.27 micromol FFA released/ml/h, P < 0.001: LPL: 7.22 +/- 3.04 versus 11.53 +/- 7.85 micromol FFA released/ml/h, P < 0.05) whereas plasma cholesteryl ester transfer protein (CETP) activity was significantly increased (8.15 +/- 1.81 versus 5.54 +/- 1.86 pmol/microl/h, P < 0.001). Both GH and IGF-I were significantly associated with HL, LPL and CETP activities. Multivariate analysis on this relatively small sample size showed that in normal subjects, triglyceride and HL activity were the major determinants of LDL-III. In contrast, GH and HDL were the main determinants in acromegaly, accounting for 32 and 24% in the variability of LDL-III respectively. In conclusion, GH excess has a direct effect on LDL subfraction distribution.
Atherosclerosis 1997 Feb 28
PMID:LDL subfractions in acromegaly: relation to growth hormone and insulin-like growth factor-I. 906 18

We measured growth hormone-related substances in patients with angina pectoris precipitated by different underlying disorders. Although hyperinsulinemia was more pronounced in patients with angina pectoris secondary to atherosclerotic coronary disease than in patients with syndrome X and variant angina, we found no evidence that growth hormone-related substances including insulin-like growth factor-I are associated with coronary atherosclerosis.
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PMID:Insulin-like growth factor-I, insulin, and angina pectoris secondary to coronary atherosclerosis, vasospasm, and syndrome X. 910 13

Hutchinson-Gilford progeria syndrome (HGPS) is a rare condition with an unknown molecular defect. Patients with HGP progressively develop failure to thrive (FTT), alopecia, loss of subcutaneous fat, scleroderma, stiffening of various joints, and severe atherosclerosis. The median life span is 13 years, and the main cause of death is cardiovascular complications. There are few reports of endocrine and metabolic studies because of the rarity of this condition, and the response to long-term growth hormone (GH) treatment has not been described. We report the results of endocrine and metabolic studies performed to investigate the etiology of growth failure in five patients with HGP. Additionally, the response to nutritional therapy (NT) and GH treatment in three of these patients is presented. Our results suggest that elevated GH levels are characteristic of this disease and that an elevated basal metabolic rate (BMR) could be the cause of the FTT seen in HGP. Nonaggressive NT slightly improved weight gain and growth velocity (GV). Combined NT and GH treatment in three patients improved the GV, increased the levels of growth factors, and paradoxically resulted in decreased BMRs. However, the response to these therapies decreased over time and did not seem to prevent the progression of atherosclerotic disease.
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PMID:Response to nutritional and growth hormone treatment in progeria. 925 64


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